Causes Of Lactic Acidosis
INTRODUCTION AND DEFINITION Lactate levels greater than 2 mmol/L represent hyperlactatemia, whereas lactic acidosis is generally defined as a serum lactate concentration above 4 mmol/L. Lactic acidosis is the most common cause of metabolic acidosis in hospitalized patients. Although the acidosis is usually associated with an elevated anion gap, moderately increased lactate levels can be observed with a normal anion gap (especially if hypoalbuminemia exists and the anion gap is not appropriately corrected). When lactic acidosis exists as an isolated acid-base disturbance, the arterial pH is reduced. However, other coexisting disorders can raise the pH into the normal range or even generate an elevated pH. (See "Approach to the adult with metabolic acidosis", section on 'Assessment of the serum anion gap' and "Simple and mixed acid-base disorders".) Lactic acidosis occurs when lactic acid production exceeds lactic acid clearance. The increase in lactate production is usually caused by impaired tissue oxygenation, either from decreased oxygen delivery or a defect in mitochondrial oxygen utilization. (See "Approach to the adult with metabolic acidosis".) The pathophysiology and causes of lactic acidosis will be reviewed here. The possible role of bicarbonate therapy in such patients is discussed separately. (See "Bicarbonate therapy in lactic acidosis".) PATHOPHYSIOLOGY A review of the biochemistry of lactate generation and metabolism is important in understanding the pathogenesis of lactic acidosis [1]. Both overproduction and reduced metabolism of lactate appear to be operative in most patients. Cellular lactate generation is influenced by the "redox state" of the cell. The redox state in the cellular cytoplasm is reflected by the ratio of oxidized and reduced nicotine ad Continue reading >>
Lactic Acidosis In Diabetes*
Abstract Lactic acidosis is occasionally responsible for metabolic acidosis in diabetics. It may occur in the presence of normal blood levels of the ketone bodies, and such cases are often described as having “non-ketotic diabetic acidosis.” Lactic acid may contribute to the metabolic acidosis in patients with true diabetic ketoacidosis, but the blood lactate concentrations in these patients are not usually very high. In some patients the ketoacidosis is replaced by a lactic acidosis during treatment. This usually occurs in association with a serious underlying disorder and is associated with a poor prognosis. A transient increase in blood lactate concentration was in fact observed in most patients after the beginning of treatment, but the significance of this finding is uncertain. Full text Full text is available as a scanned copy of the original print version. Get a printable copy (PDF file) of the complete article (930K), or click on a page image below to browse page by page. Links to PubMed are also available for Selected References. These references are in PubMed. This may not be the complete list of references from this article. Continue reading >>
- American Diabetes Association® Releases 2018 Standards of Medical Care in Diabetes, with Notable New Recommendations for People with Cardiovascular Disease and Diabetes
- Leeds diabetes clinical champion raises awareness of gestational diabetes for World Diabetes Day
- Diabetes doctors: Which specialists treat diabetes?
Hyperglycaemic Crises And Lactic Acidosis In Diabetes Mellitus
Hyperglycaemic crises are discussed together followed by a separate section on lactic acidosis. DIABETIC KETOACIDOSIS (DKA) AND HYPERGLYCAEMIC HYPEROSMOLAR STATE (HHS) Definitions DKA has no universally agreed definition. Alberti proposed the working definition of “severe uncontrolled diabetes requiring emergency treatment with insulin and intravenous fluids and with a blood ketone body concentration of >5 mmol/l”.1 Given the limited availability of blood ketone body assays, a more pragmatic definition comprising a metabolic acidosis (pH <7.3), plasma bicarbonate <15 mmol/l, plasma glucose >13.9 mmol/l, and urine ketostix reaction ++ or plasma ketostix ⩾ + may be more workable in clinical practice.2 Classifying the severity of diabetic ketoacidosis is desirable, since it may assist in determining the management and monitoring of the patient. Such a classification is based on the severity of acidosis (table 1). A caveat to this approach is that the presence of an intercurrent illness, that may not necessarily affect the level of acidosis, may markedly affect outcome: a recent study showed that the two most important factors predicting mortality in DKA were severe intercurrent illness and pH <7.0.3 HHS replaces the older terms, “hyperglycaemic hyperosmolar non-ketotic coma” and “hyperglycaemic hyperosmolar non-ketotic state”, because alterations of sensoria may be present without coma, and mild to moderate ketosis is commonly present in this state.4,5 Definitions vary according to the degree of hyperglycaemia and elevation of osmolality required. Table 1 summarises the definition of Kitabchi et al.5 Epidemiology The annual incidence of DKA among subjects with type 1 diabetes is between 1% and 5% in European and American series6–10 and this incidence appear Continue reading >>
- Women in India with Gestational Diabetes Mellitus Strategy (WINGS): Methodology and development of model of care for gestational diabetes mellitus (WINGS 4)
- Olive oil in the prevention and management of type 2 diabetes mellitus: a systematic review and meta-analysis of cohort studies and intervention trials
- Difference between Diabetes Mellitus and Diabetes Insipidus
What Is A Lactic Acid Blood Test?
It’s a test that measures the amount of lactic acid (also called “lactate”) in your blood. This acid is made in muscle cells and red blood cells. It forms when your body turns food into energy. Your body relies on this energy when its oxygen levels are low. Oxygen levels might drop during an intense workout or when you have an infection or disease. Once you finish your workout or recover from the illness, your lactic acid level tends to go back to normal. But sometimes, it doesn't. Higher-than-normal lactic acid levels can lead to a condition called lactic acidosis. If it’s severe enough, it can upset your body’s pH balance, which indicates the level of acid in your blood. Lactic acidosis can lead to these symptoms: It’s a simple blood test. Your doctor will draw blood from a vein or artery using a needle. In rare cases, he may take a sample of cerebrospinal fluid from your spinal column during a procedure called a spinal tap. Normally, you don’t have to adjust your routine to prepare for the test. If your lactic acid level is normal, you don’t have lactic acidosis. Your cells are making enough oxygen. It also tells your doctor that something other than lactic acidosis is causing your symptoms. He’ll likely order other tests to find out what it is. If your lactic acid level is high, it could be caused by a number of things. Most often, it’s because you have a condition that makes it hard for you to breathe in enough oxygen. Some of these conditions could include: Severe lung disease or respiratory failure Fluid build-up in your lungs Very low red blood cell count (severe anemia) A higher-than-normal lactic acid level in your blood can also be a sign of problems with your metabolism. And, your body might need more oxygen than normal because you have o Continue reading >>
Lactic Acidosis As A Cause Of Nonketotic Acidosis In Diabetic Patients
This article has no abstract; the first 100 words appear below. SEVERE metabolic acidosis, when it occurs in diabetic patients, is generally the result of excessive hepatic production of acetoacetic and beta-hydroxybutyric acid. Exceptional cases of metabolic acidosis in diabetic patients whose urine has failed to give a positive reaction for acetoacetic acid have long been recognized.1 In certain cases increased concentrations of beta-oxybutyric acids have been demonstrated in the plasma. A failure of renal excretion of acetoacetic acid, usually attributed to shock, has been proposed as an explanation of these cases.2 , 3 In other cases examinations of the plasma or tissues for beta-oxybutyric acids by qualitative or quantitative procedures have failed . . . *From the Metabolism Division, Department of Internal Medicine, Washington University School of Medicine. We are indebted to Drs. Thomas J. Walsh, William D. Perry and Harold Roberts for permission to study and report these cases. Continue reading >>
Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus
Introduction A 49-year-old man presented to the emergency department complaining of dyspnea for 2 days. He had a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and a severe dilated cardiomyopathy. He had been hospitalized several times in the previous year for decompensated congestive heart failure (most recently, 1 month earlier). The plasma creatinine concentration was 1.13 mg/dl on discharge. Outpatient medications included insulin, digoxin, warfarin, spironolactone, metoprolol succinate, furosemide (80 mg two times per day; increased from 40 mg daily 1 month earlier), metolazone (2.5 mg daily; added 1 month earlier), and metformin (2500 mg in three divided doses; increased from 1000 mg 1 month earlier). Physical examination revealed an obese man in moderate respiratory distress. The temperature was 36.8°C, BP was 119/83 mmHg, and heart rate was 96 per minute. Peripheral hemoglobin oxygen saturation was 97% on room air, with a respiratory rate of 26 per minute. The heart rhythm was irregularly irregular; there was no S3 or murmur. Jugular venous pressure was about 8 cm. There was 1+ edema at the ankles. A chest radiograph showed cardiomegaly and central venous prominence. The N-terminal pro-B-type natriuretic peptide level was 5137 pg/ml (reference range = 1–138 pg/ml). The peripheral hemoglobin concentration was 12.5 g/dl, the white blood cell count was 12,500/µl (76% granulocytes), and the platelet count was 332,000/µL. Initial plasma chemistries are shown in Table 1. The impression was decompensated congestive heart failure. After administration of furosemide (160 mg intravenously), the urine output increased to 320 ml over the next 1 hour. There was no improvement in the dyspnea. Within 2 hours, the patient’s BP fell to 100/64 mmHg Continue reading >>
A Side Effect You Should Know About
The glucose-lowering medication metformin (Glucophage) could cause lactic acidosis if your kidneys and liver are not working efficiently. Lactic acidosis is when high levels build up in the blood of a substance called lactic acid — a chemical that is normally produced by your body in small amounts and removed by your liver and kidneys. The risk of lactic acidosis goes up if you: have heart failure or a lung ailment have kidney or liver problems drink alcohol heavily In these cases, you might not be able to take metformin. If you don't have one of these problems, you are at a very low risk for developing lactic acidosis from metformin. You should, however, contact your doctor immediately if you suddenly develop any of these symptoms of lactic acidosis: diarrhea fast and shallow breathing muscle pain or cramping weakness tiredness or unusual sleepiness You should also let your doctor know if you get the flu or any illness that results in severe vomiting, diarrhea, and/or fever, or if your intake of fluids becomes significantly reduced. Severe dehydration can affect your kidney or liver function and increase your risk of lactic acidosis from metformin. Continue reading >>
Diabetes And Metformin Faqs
Tweet Although one of the most common drugs for type 2 diabetics, Metformin can still confuse diabetic patients. This set of FAQs are intended for information purposes, and should not replace or supersede the advice of a doctor or qualified medical professional. If you have a question about diabetes and Metformin that is not covered here, please ask the community in the Diabetes forum. Should all type 2 diabetics take Meformin? One side effect of taking Metformin is lactic acidosis, and for this reason some diabetics should not take Metformin unless specifically advised to do so by their GP or diabetes healthcare team. For this reason, diabetics with kidney problems, liver problems, and heart problems are often advised to avoid Metformin. Similarly, diabetics that are dehydrated, drink alcohol a lot, or are going to have an x-ray or surgery. For some pregnant diabetics, Metformin may not be the best choice, but in all instances this should be discussed with your doctor. Can young diabetics take Metformin? Metformin has been proven in clinical trials to lower glucose levels amongst children between 10-16 years of age suffering from type 2 diabetes. Research is less conclusive about children under 10 and children taking Metformin alongside other treatments, but your diabetes health care team should be able to elaborate on this. How much Metformin should I take? This will depend entirely on your condition, and your doctor will be able to tell you how much Metformin to take, when you should take it, and how you should take it. Usually, diabetics start out on a low dose of Metformin, and this is slowly increased until blood sugar responds. Doctors often put diabetics on combination courses with other medication, including insulin. If I take Metformin, can I stop my diet and Continue reading >>
- Is It Time to Change the Type 2 Diabetes Treatment Paradigm? No! Metformin Should Remain the Foundation Therapy for Type 2 Diabetes
- The Pros and Cons of Metformin for Diabetes
- NZ case study; A citizen scientist controls autoimmune diabetes without insulin, with a low carb diet, a glucose meter, and metformin.
Lactic Acidosis
Patient professional reference Professional Reference articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use. You may find one of our health articles more useful. Description Lactic acidosis is a form of metabolic acidosis due to the inadequate clearance of lactic acid from the blood. Lactate is a byproduct of anaerobic respiration and is normally cleared from the blood by the liver, kidney and skeletal muscle. Lactic acidosis occurs when the body's buffering systems are overloaded and tends to cause a pH of ≤7.25 with plasma lactate ≥5 mmol/L. It is usually caused by a state of tissue hypoperfusion and/or hypoxia. This causes pyruvic acid to be preferentially converted to lactate during anaerobic respiration. Hyperlactataemia is defined as plasma lactate >2 mmol/L. Classification Cohen and Woods devised the following system in 1976 and it is still widely used:[1] Type A: lactic acidosis occurs with clinical evidence of tissue hypoperfusion or hypoxia. Type B: lactic acidosis occurs without clinical evidence of tissue hypoperfusion or hypoxia. It is further subdivided into: Type B1: due to underlying disease. Type B2: due to effects of drugs or toxins. Type B3: due to inborn or acquired errors of metabolism. Epidemiology The prevalence is very difficult to estimate, as it occurs in critically ill patients, who are not often suitable subjects for research. It is certainly a common occurrence in patients in high-dependency areas of hospitals.[2] The incidence of symptomatic hyperlactataemia appears to be rising as a consequence of the use of antiretroviral therapy to treat HIV infection. It appears to increase in those taking stavudine (d4T) regimens.[3] Causes of lactic acid Continue reading >>
![What Is Lactic Acidosis In Type 2 Diabetes? [causes & Solutions]](https://diabetestalk.net/images/SMmzjAWRYrkYUGaD.jpg)
What Is Lactic Acidosis In Type 2 Diabetes? [causes & Solutions]
Lactic acidosis is when lactic acid builds ups in the bloodstream faster than it can be removed. Lactic acid is produced when oxygen levels in the body drop. The most common cause of lactic acidosis is intense exercise, usually in the form of lifting weights. When you get a “pump” or “burn” in the muscle, that’s from lactic acid build-up. The Cause In Diabetics But lactic acidosis usually happens in type 2 diabetes due to a glucose-lowering medication called, Metformin (Glucophage). The risk of lactic acidosis also goes up if you: have heart failure or a lung ailment have kidney or liver problems drink alcohol Also, dehydration can affect your kidney or liver function and increase your risk of lactic acidosis, especially when taking Metformin. So, make sure you’re always hydrated with clean water. The Symptoms Typical symptoms of lactic acidosis in diabetics is: diarrhea fast and shallow breathing muscle pain or cramping weakness tiredness or unusual sleepiness If you’re feeling nausea or weakness, you should contact your doctor and do a blood test to check electrolyte levels and see if you do have lactic acidosis. The Solutions FIRST – You need to make sure you’re always hydrated. That means to drink plenty of purified water and avoid alcohol and caffeinated beverages – since both cause dehydration. SECOND – You should consider getting OFF the drug Metformin if you’re using it, which is the primary cause of the lactic acidosis. Speak to your doctor about alternatives, preferably something natural. THIRD – It’s best to control your blood sugar and glucose levels naturally – through simple life-style changes … because this is the best long-term solution without worry of negative side-effects from drugs, such as lactic acidosis or kidney an Continue reading >>
Lactic Acidosis
The buildup of lactic acid in the bloodstream. This medical emergency most commonly results from oxygen deprivation in the body’s tissues, impaired liver function, respiratory failure, or cardiovascular disease. It can also be caused by a class of oral diabetes drugs called biguanides, which includes metformin (brand name Glucophage). Another biguanide called phenformin was pulled from the market in the United States in 1977 because of an unacceptably high rate of lactic acidosis associated with its use. Concerns about lactic acidosis also delayed the introduction of metformin to the U.S. market until 1995, despite the fact that it had been widely used for years in other countries. There have been reports of lactic acidosis occurring in people taking metformin, and the U.S. Food and Drug Administration estimates that lactic acidosis occurs in 5 out of every 100,000 people who use metformin for any length of time. However, this risk is much lower than it was in people taking phenformin, and it is not clear whether the episodes of lactic acidosis associated with metformin have actually been due to metformin use. In fact, the lactic acidosis could have been explained by the person’s diabetes and related medical conditions. Nonetheless, diabetes experts recommend that metformin not be used in people with congestive heart failure, kidney disease, or liver disease. They also recommend that it be discontinued (at least temporarily) in people undergoing certain medical imaging tests called contrast studies. Symptoms of lactic acidosis include feeling very weak or tired or having unusual muscle pain or unusual stomach discomfort. Continue reading >>
Lactic Acidosis In A Patient With Type 2 Diabetes Mellitus
Go to: Introduction A 49-year-old man presented to the emergency department complaining of dyspnea for 2 days. He had a history of hypertension, type 2 diabetes mellitus, atrial fibrillation, and a severe dilated cardiomyopathy. He had been hospitalized several times in the previous year for decompensated congestive heart failure (most recently, 1 month earlier). The plasma creatinine concentration was 1.13 mg/dl on discharge. Outpatient medications included insulin, digoxin, warfarin, spironolactone, metoprolol succinate, furosemide (80 mg two times per day; increased from 40 mg daily 1 month earlier), metolazone (2.5 mg daily; added 1 month earlier), and metformin (2500 mg in three divided doses; increased from 1000 mg 1 month earlier). Physical examination revealed an obese man in moderate respiratory distress. The temperature was 36.8°C, BP was 119/83 mmHg, and heart rate was 96 per minute. Peripheral hemoglobin oxygen saturation was 97% on room air, with a respiratory rate of 26 per minute. The heart rhythm was irregularly irregular; there was no S3 or murmur. Jugular venous pressure was about 8 cm. There was 1+ edema at the ankles. A chest radiograph showed cardiomegaly and central venous prominence. The N-terminal pro-B-type natriuretic peptide level was 5137 pg/ml (reference range = 1–138 pg/ml). The peripheral hemoglobin concentration was 12.5 g/dl, the white blood cell count was 12,500/µl (76% granulocytes), and the platelet count was 332,000/µL. Initial plasma chemistries are shown in Table 1. The impression was decompensated congestive heart failure. After administration of furosemide (160 mg intravenously), the urine output increased to 320 ml over the next 1 hour. There was no improvement in the dyspnea. Within 2 hours, the patient’s BP fell to 100/ Continue reading >>
Biochemistry - Why Would Lactate Be High In Diabetics? - Biology Stack Exchange
Why are lactate level high in diabetes? For example, type II diabetes are resistant to insulin. If those patients are insulin resistant their gluconeogenesis should be working at a high rate and, because of that, lactate uptake by the liver should be removing lactate from the blood. Alternatively, type I diabetics don't produce insulin, so the ratio insulin/glucagon would always be very low and gluconeogenesis should be stimulated... So I don't understand why lactate levels are high in diabetes... Can someone help me? Can you provide any references in support of your assertion that diabetes is associated with elevated levels of lactate? Alan Boyd Jan 7 '14 at 19:43 It was just an experiment that we did in school, with diabetic rats and normal rats. Diabetic rats had higher levels of lactate and my professor said that it is because the diabetic rats don't do gluconeogenesis and so, lactate accumulates in the plasma... But it doesn't make sense for me! user5354 Jan 7 '14 at 19:46 This condition is also known as "lactic acidosis" and can be pretty dangerous, since it influences the pH of the blood. When we metabolize glucose to produce ATP and NADH it is metabolized finally to pyruvate in a process called glyolysis (I am not going into detail here since this is nicely explained in the Wikipedia). Pyruvate can then be used further in the body in the Gluconeogenesis , the Citric acid cycle and other pathways. If a lot of energy is needed Pyruvate is converted by the pyruvate dehydrogenase into acetyl-CoA. The problem with diabetes is that the pyruvate dehydrogenase can be inhibited in diabetes. If the body then needs a lot of energy pyruvate will be converted into lactate which is released by the cells into the bloodstream.Gluconeogenesis cannot be activated since this need Continue reading >>
Lactic Acidosis
A.D.A.M., Inc. is accredited by URAC, also known as the American Accreditation HealthCare Commission (www.urac.org). URAC's accreditation program is an independent audit to verify that A.D.A.M. follows rigorous standards of quality and accountability. A.D.A.M. is among the first to achieve this important distinction for online health information and services. Learn more about A.D.A.M.'s editorial policy, editorial process and privacy policy. A.D.A.M. is also a founding member of Hi-Ethics and subscribes to the principles of the Health on the Net Foundation (www.hon.ch). The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions. Call 911 for all medical emergencies. Links to other sites are provided for information only -- they do not constitute endorsements of those other sites. Copyright 1997-2018, A.D.A.M., Inc. Duplication for commercial use must be authorized in writing by ADAM Health Solutions. Continue reading >>
Metformin And Fatal Lactic Acidosis
Publications Published: July 1998 Information on this subject has been updated. Read the most recent information. Dr P Pillans,former Medical Assessor, Centre for Adverse Reactions Monitoring (CARM), Dunedin Metformin is a useful anti-hyperglycaemic agent but significant mortality is associated with drug-induced lactic acidosis. Significant renal and hepatic disease, alcoholism and conditions associated with hypoxia (eg. cardiac and pulmonary disease, surgery) are contraindications to the use of metformin. Other risk factors for metformin-induced lactic acidosis are sepsis, dehydration, high dosages and increasing age. Metformin remains a major reported cause of drug-associated mortality in New Zealand. Of the 12 cases of lactic acidosis associated with metformin reported to CARM since 1977, 2 occurred in the last year and 8 cases had a fatal outcome. Metformin useful but small risk of potentially fatal lactic acidosis Metformin is a useful therapeutic agent for obese non-insulin dependent diabetics and those whose glycaemia cannot be controlled by sulphonylurea monotherapy. Lactic acidosis is an uncommon but potentially fatal adverse effect. The reported frequency of lactic acidosis is 0.06 per 1000 patient-years, mostly in patients with predisposing factors.1 Examples of metformin-induced lactic acidosis cases reported to CARM include: A 69-year-old man, with renal and cardiac disease, was prescribed metformin due to failing glycaemic control on glibenclamide monotherapy. He was well for six weeks, then developed lactic acidosis and died within 3 days. Post-surgical lactic acidosis caused the death of a 70-year-old man whose metformin was not withdrawn at the time of surgery. A 56-year-old woman, with no predisposing disease, died from lactic acidosis following major Continue reading >>
